Fluid and Electrolytes: Balance and Disturbance Dr. Abdul-Monim Batiha

Fluid and Electrolyte Balance Necessary for life, homeostasis Nursing role: help prevent, treat fluid, electrolyte disturbances

Fluid Approximately 60% of typical adult is fluid Varies with age, body size, gender Intracellular fluid Extracellular fluid Intravascular: the fluid within the blood vessels e.g. plazma Interstitial: fluid surrounds the cell (e.g. lymph Transcellular: cerebrospinal, pericardial, synovial, intraocular, pleural, sweat and digestive secretion “Third spacing”: loss of ECF into space that does not contribute to equilibrium

Electrolytes Active chemicals that carry positive (cations), negative (anions) electrical charges Major cations: sodium, potassium, calcium, magnesium, hydrogen ions Major anions: chloride, bicarbonate, phosphate, sulfate, and proteinate ions Electrolyte concentrations differ in fluid compartments

Regulation of Fluid Movement of fluid through capillary walls depends on Hydrostatic pressure: exerted on walls of blood vessels Osmotic pressure: exerted by protein in plasma Direction of fluid movement depends on differences of hydrostatic, osmotic pressure

Regulation of Fluid Osmosis: area of low solute concentration to area of high solute concentration Diffusion: solutes move from area of higher concentration to one of lower concentration Filtration: movement of water, solutes occurs from area of high hydrostatic pressure to area of low hydrostatic pressure Active transport: physiologic pump that moves fluid from area of lower concentration of one of higher concentration

Active Transport Physiologic pump that moves fluid from area of lower concentration to one of higher concentration Movement against concentration gradient Sodium-potassium pump: maintains higher concentration of extracellular sodium, intracellular potassium Requires adenosine (ATP) for energy

Question Tell whether the following statement is true or false: Osmosis is the movement of a substance from an area of higher concentration to one of lower concentration.

Answer False. Rationale: Diffusion is the movement of a substance from an area of higher concentration to one of lower concentration. The concentration of dissolved substances draws fluid in that direction. Osmosis is the movement of fluid, through a semipermeable membrane, from an area of low solute concentration to an area of high solute concentration until the solutions are of equal concentration.

Routes of Gains and Losses Dietary intake of fluid, food or enteral feedingIngested fluid (60%) and solid food (30%) Metabolic water or water of oxidation (10%) Parenteral fluids

Routes of Gains and Losses (cont’d) Kidney: urine output Skin loss: sensible, insensible losses Lungs GI tract Other Urine (60%) and feces (4%) Insensible losses (28%), sweat (8%)

Water Intake and Output Figure 26.4 Chapter 26: Fluid, Electrolyte, and Acid-Base Balance

Question What is the average daily urinary output in an adult? 0.5 L

Answer C. 1.5 L Rationale: Vital to the regulation of fluid and electrolyte balance, the kidneys normal filter 170 L of plasma every day in the adult, while excreting only 1.5 L of urine.

Regulation of Water Intake The hypothalamic thirst center is stimulated: By a decline in plasma volume of 10%–15% By increases in plasma osmolality of 1–2% Via baroreceptor input, angiotensin II, and other stimuli

Thirst is reduced as soon as we begin to drink water Feedback signals that inhibit the thirst centers include: Moistening of the mucosa of the mouth and throat Activation of stomach and intestinal stretch receptors

Regulation of Water Output Obligatory water losses include: Insensible water losses from lungs and skin Water that accompanies undigested food residues in feces Obligatory water loss reflects the fact that: Kidneys excrete 900-1200 mOsm of solutes to maintain blood homeostasis Urine solutes must be flushed out of the body in water

Influence and Regulation of ADH Water reabsorption in collecting ducts is proportional to ADH release Low ADH levels produce dilute urine and reduced volume of body fluids High ADH levels produce concentrated urine Hypothalamic osmoreceptors trigger or inhibit ADH release Factors that specifically trigger ADH release include prolonged fever; excessive sweating, vomiting, or diarrhea; severe blood loss; and traumatic burns

Mechanisms and Consequences of ADH Release Figure 26.6

Fluid Volume Imbalances Fluid volume deficit (FVD): hypovolemia Fluid volume excess (FVE): hypervolemia

Fluid Volume Deficit Loss of extracellular fluid exceeds intake ratio of water Electrolytes lost in same proportion as they exist in normal body fluids Dehydration: loss of water along with increased serum sodium level May occur in combination with other imbalances

Fluid Volume Deficit (cont’d) Dehydration Causes: fluid loss from vomiting, diarrhea, GI suctioning, sweating, decreased intake, inability to gain access to fluid Risk factors: diabetes insipidus, adrenal insufficiency, osmotic diuresis, hemorrhage, coma,

Fluid Volume Deficit (cont’d) Manifestations: rapid weight loss, decreased skin turgor, oliguria, concentrated urine, postural hypotension, rapid weak pulse, increased temperature, cool clammy skin due to vasoconstriction, lethargy, thirst, nausea, muscle weakness, cramps Laboratory data: elevated BUN in relation to serum creatinine, increased hematocrit Serum electrolyte changes may occur

Fluid Volume Deficit (cont’d) Medical management: provide fluids to meet body needs Oral fluids IV solutions (isotonic electrolytes solution; e.g. ringer lactate solution or 0.9 sodium chloride)

Fluid Volume Deficit - Nursing Management I&O, VS Monitor for symptoms: skin and tongue turgor, mucosa, UO, mental status Measures to minimize fluid loss Oral care Administration of oral fluids Administration of parenteral fluids

Question What is a major indicator of extracellular FVD? Full and bounding pulse Drop in postural blood pressure Elevated temperature Pitting edema of lower extremities

Answer B. Drop in postural blood pressure Rationale: FVD signs and symptoms include acute weight loss; decreased skin turgor; oliguria; concentrated urine; orthostatic hypotension due to volume depletion; a weak, rapid heart rate; flattened neck veins; increased temperature; thirst; decreased or delayed capillary refill; decreased central venous pressure; cool, clammy, pale skin related to peripheral vasoconstriction; anorexia; nausea; lassitude; muscle weakness; and cramps. Clinical manifestations of FVE result from expansion of the ECF and include edema, distended neck veins, and crackles (abnormal lung sounds).

Fluid Volume Excess Due to fluid overload or diminished homeostatic mechanisms Risk factors: heart failure, renal failure, cirrhosis of liver Contributing factors: excessive dietary sodium or sodium-containing IV solutions Manifestations: edema, distended neck veins, abnormal lung sounds (crackles), tachycardia, increased BP, pulse pressure and CVP, increased weight, increased UO, shortness of breath and wheezing Medical management: directed at cause, restriction of fluids and sodium, administration of diuretics

Disorders of Water Balance: Edema Atypical accumulation of fluid in the interstitial space, leading to tissue swelling Caused by anything that increases flow of fluids out of the bloodstream or hinders their return Factors that accelerate fluid loss include: Increased blood pressure, capillary permeability Incompetent venous valves, localized blood vessel blockage Congestive heart failure, hypertension, high blood volume

Edema Hindered fluid return usually reflects an imbalance in colloid osmotic pressures Hypoproteinemia – low levels of plasma proteins Forces fluids out of capillary beds at the arterial ends Fluids fail to return at the venous ends Results from protein malnutrition, liver disease, or glomerulonephritis

Edema Chapter 26: Fluid, Electrolyte, and Acid-Base Balance Blocked (or surgically removed) lymph vessels: Cause leaked proteins to accumulate in interstitial fluid Exert increasing colloid osmotic pressure, which draws fluid from the blood Interstitial fluid accumulation results in low blood pressure and severely impaired circulation Chapter 26: Fluid, Electrolyte, and Acid-Base Balance

Fluid Volume Excess - Nursing Management I&O and daily weights; assess lung sounds, edema, other symptoms; monitor responses to medications- diuretics Promote adherence to fluid restrictions, patient teaching related to sodium and fluid restrictions Monitor, avoid sources of excessive sodium, including medications Promote rest Semi-Fowler’s position for orthopnea Skin care, positioning/turning

Electrolyte Imbalances Sodium: hyponatremia, hypernatremia Potassium: hypokalemia, hyperkalemia Calcium: hypocalcemia, hypercalcemia Magnesium: hypomagnesemia, hypermagnesemia Phosphorus: hypophosphatemia, hyperphosphatemia Chloride: hypochloremia, hyperchloremia

Hyponatremia Serum sodium less than 135 mEq/L Causes: adrenal insufficiency, water intoxication, SIADH (Syndrome of inappropriate ADH secretion) or losses by vomiting, diarrhea, sweating, diuretics Manifestations: poor skin turgor, dry mucosa, headache, decreased salivation, decreased BP, nausea, abdominal cramping, neurologic changes Medical management: water restriction, sodium replacement Nursing management: assessment and prevention, dietary sodium and fluid intake, identify and monitor at- risk patients, effects of medications (diuretics, lithium)

Hypernatremia Serum sodium greater than 145mEq/L Causes: excess water loss, excess sodium administration, diabetes insipidus, heat stroke, hypertonic IV solutions Manifestations: thirst; elevated temperature; dry, swollen tongue; sticky mucosa; neurologic symptoms; restlessness; weakness Note: thirst may be impaired in elderly or the ill Medical management: hypotonic electrolyte solution or D5W Nursing management: assessment and prevention, assess for OTC (Over the counter drugs) sources of sodium, offer and encourage fluids to meet patient needs, provide sufficient water with tube feedings

Hypokalemia Below-normal serum potassium (<3.5 mEq/L), may occur with normal potassium levels with alkalosis due to shift of serum potassium into cells Causes: GI losses, medications, alterations of acid-base balance, hyperaldosterism, poor dietary intake Manifestations: fatigue, anorexia, nausea, vomiting, dysrhythmias, muscle weakness and cramps, paresthesias, glucose intolerance, decreased muscle strength and DTRs Medical management: increased dietary potassium, potassium replacement, IV for severe deficit Nursing management: assessment, severe hypokalemia is life-threatening, monitor ECG and ABGs, dietary potassium, nursing care related to IV potassium administration

Hyperkalemia Serum potassium greater than 5.0 mEq/L Causes: usually treatment related, impaired renal function, hypoaldosteronism, tissue trauma, acidosis Manifestations: cardiac changes and dysrhythmias, muscle weakness with potential respiratory impairment, paresthesias, anxiety, GI manifestations Medical management: monitor ECG, limitation of dietary potassium, cation-exchange resin (Kayexalate), IV sodium bicarbonate , IV calcium gluconate, regular insulin and hypertonic dextrose IV, -2 agonists, dialysis

Hyperkalemia (cont’d) Nursing management: assessment of serum potassium levels, mix IVs containing K+ well, monitor medication affects, dietary potassium restriction/dietary teaching for patients at risk Hemolysis of blood specimen or drawing of blood above IV site may result in false laboratory result Salt substitutes, medications may contain potassium Potassium-sparing diuretics may cause elevation of potassium Should not be used in patients with renal dysfunction

Question Tell whether the following statement is true or false: The ECG change that is specific to hyperkalemia is a peaked T wave.

Answer True. Rationale: The ECG changes that are specific to hyperkalemia are peaked T wave; wide, flat P wave; and wide QRS complex. The ECG changes that are specific to hypokalemia are flatted T wave and the appearance of a U wave.

Hypocalcemia Serum level less than 8.5 mg/dL, must be considered in conjunction with serum albumin level Causes: hypoparathyroidism, malabsorption, pancreatitis, alkalosis, massive transfusion of citrated blood, renal failure, medications, other Manifestations: tetany, circumoral numbness, paresthesias, hyperactive DTRs, Trousseau’s sign, Chovstek's sign, seizures, respiratory symptoms of dyspnea and laryngospasm, abnormal clotting, anxiety

Hypocalcemia (cont’d) Medical management: IV of calcium gluconate, calcium and vitamin D supplements; diet Nursing management: assessment, severe hypocalcemia is life-threatening, weight-bearing exercises to decrease bone calcium loss, patient teaching related to diet and medications, and nursing care related to IV calcium administration

Trousseau’s Sign

Hypercalcemia 9-11 Serum level above 11 mg/dL Causes: malignancy and hyperparathyroidism, bone loss related to immobility Manifestations: muscle weakness, incoordination, anorexia, constipation, nausea and vomiting, abdominal and bone pain, polyuria, thirst, ECG changes, dysrhythmias Medical management: treat underlying cause, fluids, furosemide, phosphates, calcitonin, biphosphonates Nursing management: assessment, hypercalcemic crisis has high mortality, encourage ambulation, fluids of 3 to 4 L/d, provide fluids containing sodium unless contraindicated, fiber for constipation, ensure safety

Hypomagnesemia ( normal 1.8-3) Serum level less than 1.8 mg/dL, evaluate in conjunction with serum albumin Causes: alcoholism, GI losses, enteral or parenteral feeding deficient in magnesium, medications, rapid administration of citrated blood; contributing causes include diabetic ketoacidosis, sepsis, burns, hypothermia Manifestations: neuromuscular irritability, muscle weakness, tremors, ECG changes and dysrhythmias, alterations in mood and level of consciousness Medical management: diet, oral magnesium, magnesium sulfate IV

Hypomagnesemia (cont’d) Nursing management: assessment, ensure safety, patient teaching related to diet, medications, alcohol use, and nursing care related to IV magnesium sulfate Hypomagnesemia often accompanied by hypocalcemia Need to monitor, treat potential hypocalcemia Dysphasia common in magnesium-depleted patients Assess ability to swallow with water before administering food or medications

Hypermagnesemia Serum level more than 2.7 mg/dL Causes: renal failure, diabetic ketoacidosis, excessive administration of magnesium Manifestations: flushing, lowered BP, nausea, vomiting, hypoactive reflexes, drowsiness, muscle weakness, depressed respirations, ECG changes, dysrhythmias Medical management: IV calcium gluconate, loop diuretics, IV NS of RL, hemodialysis Nursing management: assessment, do not administer medications containing magnesium, patient teaching regarding magnesium containing Over-the-counter drug.

Hypophosphatemia (normal 3-4.5) Serum level below 2.5 mg/DL Causes: alcoholism, refeeding of patients after starvation, pain, heat stroke, respiratory alkalosis, hyperventilation, diabetic ketoacidosis, hepatic encephalopathy, major burns, hyperparathyroidism, low magnesium, low potassium, diarrhea, vitamin D deficiency, use of diuretic and antacids Manifestations: neurologic symptoms, confusion, muscle weakness, tissue hypoxia, muscle and bone pain, increased susceptibility to infection Medical management: oral or IV phosphorus replacement Nursing management: assessment, encourage foods high in phosphorus, gradually introduce calories for malnourished patients receiving parenteral nutrition

Hyperphosphatemia Serum level above 4.5 mg/DL Causes: renal failure, excess phosphorus, excess vitamin D, acidosis, hypoparathyroidism, chemotherapy Manifestations: few symptoms; soft-tissue calcifications, symptoms occur due to associated hypocalcemia Medical management: treat underlying disorder, vitamin- D preparations, calcium-binding antacids, phosphate- binding gels or antacids, loop diuretics, NS IV, dialysis Nursing management: assessment, avoid high- phosphorus foods; patient teaching related to diet, phosphate-containing substances, signs of hypocalcemia

Hypochloremia Serum level less than 96 mEq/L Causes: Addison’s disease, reduced chloride intake, GI loss, diabetic ketoacidosis, excessive sweating, fever, burns, medications, metabolic alkalosis Loss of chloride occurs with loss of other electrolytes, potassium, sodium Manifestations: agitation, irritability, weakness, hyperexcitability of muscles, dysrhythmias, seizures, coma Medical management: replace chloride-IV NS or 0.45% NS Nursing management: assessment, avoid free water, encourage high-chloride foods, patient teaching related to high-chloride foods

Hyperchloremia (96-109) Serum level more than 108 mEq/L Causes: excess sodium chloride infusions with water loss, head injury, hypernatremia, dehydration, severe diarrhea, respiratory alkalosis, metabolic acidosis, hyperparathyroidism, medications Manifestations: tachypnea, lethargy, weakness, rapid, deep respirations, hypertension, cognitive changes Normal serum anion gap Medical management: restore electrolyte and fluid balance, LR, sodium bicarbonate, diuretics Nursing management: assessment, patient teaching related to diet and hydration

Maintaining Acid-Base Balance Normal plasma pH 7-35-7.45: hydrogen ion concentration Major extracellular fluid buffer system; bicarbonate-carbonic acid buffer system Kidneys regulate bicarbonate in ECF Lungs under control of medulla regulate CO2, carbonic acid in ECF

Maintaining Acid-Base Balance (cont’d) Other buffer systems ECF: inorganic phosphates, plasma proteins ICF: proteins, organic, inorganic phosphates Hemoglobin

Question What is the most common buffer system in the body? Plasma protein Hemoglobin Phosphate Bicarbonate-carbonic acid

Answer D. Bicarbonate-carbonic acid Rationale: The body’s major extracellular buffer system is the bicarbonate–carbonic acid buffer system, which is assessed when arterial blood gases are measured.

Metabolic Acidosis Low pH <7.35 Low bicarbonate <22 mEq/L Most commonly due to renal failure Manifestations: headache, confusion, drowsiness, increased respiratory rate and depth, decreased blood pressure, decreased cardiac output, dysrhythmias, shock; if decrease is slow, patient may be asymptomatic until bicarbonate is 15 mEq/L or less Correct underlying problem, correct imbalance Bicarbonate may be administered

Metabolic Acidosis (cont’d) With acidosis, hyperkalemia may occur as potassium shifts out of cell As acidosis is corrected, potassium shifts back into cell, potassium levels decrease Monitor potassium levels Serum calcium levels may be low with chronic metabolic acidosis Must be corrected before treating acidosis

Metabolic Alkalosis High pH >7.45 High bicarbonate >26 mEq/L Most commonly due to vomiting or gastric suction May also be due to medications, especially long-term diuretic use Hypokalemia will produce alkalosis Manifestations: symptoms related to decreased calcium, respiratory depression, tachycardia, symptoms of hypokalemia

Metabolic Alkalosis (cont’d) Correct underlying disorder, supply chloride to allow excretion of excess bicarbonate, restore fluid volume with sodium chloride solutions

Respiratory Acidosis Low pH <7.35 PaCO2 >42 mm Hg Always due to respiratory problem with inadequate excretion of CO2 With chronic respiratory acidosis, body may compensate, may be asymptomatic Symptoms may be suddenly increased pulse, respiratory rate and BP, mental changes, feeling of fullness in head

Respiratory Acidosis (cont’d) Potential increased intracranial pressure Treatment aimed at improving ventilation

Respiratory Alkalosis High pH >7.45 PaCO2 <35 mm Hg Always due to hyperventilation Manifestations: lightheadedness, inability to concentrate, numbness and tingling, sometimes loss of consciousness Correct cause of hyperventilation

Arterial Blood Gases pH 7.35 - (7.4) - 7.45 PaCO2 35 - (40) - 45 mm Hg HCO3ˉ 22 - (24) - 26 mEq/L Assumed average values for ABG interpretation PaO2 80 to 100 mm Hg Oxygen saturation >94% Base excess/deficit ±2 mEq/L

Parenteral fluid therapy Purpose: 1- to provide water, electrolytes, and nutrition to meet daily requirements. 2- to replace water and correct electrolytes imbalance 3- to administer medication and blood products

Types Isotonic fluids: which have a total osmolality close to that of the ECF and does not effect on RBC. 1 lit of these solutions expand the ECF by 1 lit and the plasma by 0.25 lit 1- D5W: used for supply water and increase serum osmolality; don't administer it during fluid resuscitation bcz of hyperglycemia About 1lit of D5W provides fewer than 200 kcal 2- normal saline: (0.9%): used to correct the EC volume defect, within blood administration, to replace sodium losses in case of burn. - Not used for HF, PE, Renal impairment, sodium retention

Types (cont…) 3- other solutions: Lactated Ringers; contains potassium, calcium, and sodium chloride. Used to correct dehydration, sodium depletion, and replace GI losses Hypotonic fluids: used to replace cellular fluid, provide free water to excrete the body wastes, treat hypernatremia and other hyperosmolar conditions. 1- half strength saline (0.45% sodium chloride) SE of the excessive use of hypotonic solutions leads to intravascular fluids depletion, decrease BP, cellular edema, and cell damage

Hypertonic fluids: when normal saline and Lactated ringer’s contains 5% dextrose, the total osmolality exceed that the ECF Other IV substances: When the patient is unable to tolerate food, nutritional requirements are often met using IV route - e.g. 50% dextrose in water. Protein, or fat,

hypertonic A solution that exerts a higher osmotic pressure than that of blood plasma. Administration of this fluid increases the solute concentration of plasma, drawing water out of the cells and into the extracellular compartment to restore osmotic equilibrium; cells will then shrink. 1. D5W in normal saline solution. 2. D5W in half normal saline solution (only slightly hypertonic because dextrose is rapidly metabolized and renders only temporary osmotic pressure).

3. Dextrose 10% in water. 4. Dextrose 20% in water. 5. 3% or 5% sodium chloride solution. 6. Hyperalimentation solutions. 7. D5W in lactated Ringer’s solution. 8. Albumin 25%.

IV Site Selection

Complications of IV Therapy Fluid overload, Air embolism Septicemia, other infections Infiltration: is the unintentional administration of nonvesicant solutions or medication into surrounding tissue as a result of dislodges or perforates the wall of the veins ,

extravasation: similar to Infiltration with an inadvertent administration of vesicant or irritant solution Phlebitis Thrombophlebitis Hematoma Clotting, obstruction

Composition of Fluids 1. Saline solutions—water and electrolytes (Na+, Cl−). 2. Dextrose solutions—water or saline and calories. 3. Lactated Ringer’s solution—water and electrolytes (Na+, K+,Cl−, Ca++, lactate). 4. Balanced isotonic solution—varies; water, some calories, electrolytes(Na+, K+, Mg++, Cl−, HCO3−, gluconate).

5. Whole blood and blood components. 6. Plasma expanders—albumin, mannitol, dextran, plasma protein fraction 5%, hetastarch; exert increased oncotic pressure, pulling fluid from interstitium into the circulation and temporarily increasing blood volume. 7. Parenteral hyperalimentation—fluid, electrolytes, amino acids, and calories.

Uses and Precautions with Common Types of Infusions 1. D5W a. Used to replace water (hypotonic fluid) losses, supply some caloric intake, or administer as carrying solution for numerous medications. b. Should be used cautiously in patients with water intoxication (hyponatremia, syndrome of inappropriate antidiuretic hormone release). Should not be used as concurrent solution infusion with blood or blood components.

2. Normal saline solution a. Used to replace saline (isotonic fluid) losses, administer with blood components, or treat patients in hemodynamic shock. b. Should be used cautiously in patients with isotonic volume excess (heart failure, renal failure). 3. Lactated Ringer’s solution a. Used to replace isotonic fluid losses, replenish specific electrolyte losses, and moderate metabolic acidosis. Use cautiously in patients with liver failure.